Salvucci 09-13-07 Clinical Aspects Of Cad

Front 1

The ischemic cascade ?

Back 1

increased lvedp→
wall motion abnormality→
st segment changes→
angina

Front 2

Clinical coronary ischemic events (MI, angina) almost always implies _______.

Back 2

LV ischemia

--May have concomitant RV and/or atrial infarction also

Front 3

As a general rule, which wall MI has a higher morbidity and mortality?

Back 3

anterior

Front 4

muscles-infarcted mitral papillary muscles can result in mitral regurgitation
More common in ______ wall MI (pm papillary muscle)

Back 4

inferior

Front 5

Septal MI can result in ____

Back 5

VSD

Front 6

Symptoms of ischemia

Back 6

Angina (Greek: choking)
Dyspnea
Diaphoresis
Nausea
Fatigue/weakness/faintness
Arrhythmia symptoms

Front 7

Radiation of angina pectoris

Back 7

Left arm, possible right or both, throat, jaw, intrascapular

Front 8

Duration of angina pectoris

Back 8

Classic is 2 to 5 minutes. Remember, pt’s perception of time is distorted. Rarely if ever less than a minute.

Front 9

Relief of angina pectoris

Back 9

Rest, nitroglycerine (ntg relief is very fast; pts relieved by ntg in 10 or 15 minutes is not a ntg effect)

Front 10

Prinzmetal’s Angina is Chest pain secondary to _____.

Back 10

coronary artery spasm

Front 11

is there atherosclerotic obstructive disease in Prinzmetal’s Angina?

Back 11

Usually no significant atherosclerotic obstructive disease

Front 12

ECG finding in Prinzmetal’s Angina

Back 12

Hallmark is ST segment elevation during an occurrence of chest pain

Front 13

When does Prinzmetal's angina occur?

Back 13

Occurs at rest
Usually early AM hours

Front 14

Segmental or global wall motion abnormalities secondary to acute, relatively short occurring ischemia. Viable myocardium with potential for reversibility

Back 14

Myocardial Stunning

Front 15

Segmental or global wall motion abnormalities secondary to chronic ischemia. Viable myocardium with potential for reversibility. Differentiate from CMO and infarcted tissue (PET scan)

Back 15

Myocardial Hibernation

Front 16

How to reverse wall motion abnormalities?

Back 16

Revascularization will usually result in improved or complete recovery of wall motion abnormalities
May take several months to reverse

Front 17

CMO?

Back 17

cardiomyopathy

Front 18

Stress testing
Treadmill only

Comment on sensitivity and specificity

Back 18

Sensitivity and specificity low. High false positives in women

Front 19

Nuclear Stress testing -

comment on sensitivity and specificity

Back 19

Highly sensitive and specific

Front 20

Can assess LVEF response to exercise

a) treadmill stress test
b) nuclear stress test

Back 20

nuclear stress test

Front 21

Downside to nuclear stress test

Back 21

Expensive, time consuming, requires pt cooperation, radiation exposure

Front 22

Stress Testing For patients unable to walk adequately on a treadmill

Back 22

Pharmacologic Stress Testing

Front 23

Agents “stress” the heart and can provide equal assessment to exercise testing for ischemia

Back 23

Adenosine, dipyrimidole with nuclear

Front 24

Pharm Stress test type:
Chronotropic/inotropic stress, also provides equally good assessment of ischemia

Back 24

Dobutamine with nuclear or Echo

Front 25

Stress test type:
Evaluation of new wall motion abnormalities compared to rest as a sign of ischemia
Equal sensitivity and specificity to nuclear stress testing

Back 25

Echocardiographic stress test

Front 26

Same quality, location, related symptoms, etc as stable angina but occurs with little or no exertion, or represents a marked change in pattern from the pts stable condition (occurring with less activity, more frequent, more intense, persists for longer periods of time)

Back 26

Unstable Angina Pectoris

Front 27

Unstable symptoms with positive enzyme elevation and no st segment elevation on the ECG
Old names include sub-endocardial MI, and non-Q wave MI
Early mortality and morbidity less than STEMI but 1 year M&M begins to catch up

Back 27

Non ST segment elevation MI

Front 28

what differentiates NSTEMI and unstable angina pectoris?

Back 28

Elevation of cardiac enzymes differentiates NSTEMI and UAP
Consider these entities as a continuum

Front 29

As the name states, must have ECG st segment elevation criteria for diagnosis, along with cardiac enzyme elevation

Back 29

ST Segment MI

Front 30

Not all st segment elevation on an ECG constitutes infarction (consider pericarditis, early repolarization, _______.)

Back 30

bundle branch blocks, hypertrophy, spasm

Front 31

Usually means transmural injury, old names transmural MI, Q wave infarct

Back 31

ST Segment MI

Front 32

Physical Findings of MI

Back 32

Persistent anginal pain, dyspnea, diaphoresis
Acute distress, clammy skin, exam may be normal, or may include S4 or S3 gallop, murmur of MR or VSD, neck vein distention, pulmonary rales, low blood pressure

Front 33

ECG findings of MI

Back 33

Classic st segment elevation (fireman’s hat), st segment depression and/or t wave inversion, arrhythmias, heart block, tachy or bradycardia

Front 34

Echo findings of MI

Back 34

Wall motion abnormality, MR, VSD

Front 35

CXR of MI

Back 35

Look for CHF (edema)

Front 36

Cardiac catheterization of MI

Back 36

LV wall motion abnormality, occluded, or near occluded vessel
STEMI usually results from total vessel occlusion
NSTEMI and UAP usually results from sub total occlusion, or total occlusion with collaterals

Front 37

Labs of MI

Back 37

Cardiac marker enzymes are the mainstay of diagnosis
Troponin I and T are the most specific, very sensitive (false elevations occur
Elevation of CK, SGOT, LDH-much less clinical utility

Front 38

Myocardial InfarctionTreatment

(ins company is watching you!)

Back 38

Oxygen
Rest
Pain management
Anxiolytic
Blood pressure control
Anti-platelet (ASA is mainstay, plavix, IIb-IIIa agents)
B blockers, if no contra-indications
Nitroglycerine
Heparin (unfractionated)
ST segment MI, or new LBBB: fibrinolytic, if no contra, and no plan for immediate cath and intervention
Non ST segment MI: Glycoprotein IIb-IIIa agent
Intensive care unit
Potential additional pharm agents: Plavix, ACE-I, coumadin, statin, anti-arrhythmics

Front 39

The ultimate predictor of morbidity and mortality is infarct size: often reflected as what heart parameter

Back 39

ejection fraction.

Front 40

Acute Coronary Revascularization
treatments

Back 40

PTCI: balloon angioplasty, stents

Front 41

treatment of Ventricular Arrhythmias post-MI

Back 41

Lidocaine, amiodarone

Front 42

Polymorphic VT usually indicates ________ mediated

Back 42

ischemia

Front 43

Monomorphic VT usually secondary to __________

Back 43

scar tissue

Front 44

Treatment of CHF post-MI

Back 44

diuresis, morphine, afterload reduction, possible need for positive inotrope